Hepatic fibrosis is a condition in which production of fiber tissues called extracellular matrix composed of collagen and glycoconjugates is promoted in the process of repairing hepatocytes necrotized by various hepatic disorders such as viral hepatitis, alcoholic hepatopathy, autoimmune hepatopathy, metabolic hepatopathy and the like, and these fiber tissues are gradually accumulated along with the progression of the disease.
Particularly, after infection with hepatitis C virus (HCV), persistent infection occurs easily and chronic hepatitis is developed. Chronic hepatitis progresses to hepatic fibrosis, in which production of matrix exceeds decomposition and absorption thereof, and accumulation of fiber tissues continues, and gradually progresses to cirrhosis in which liver becomes hard due to fiber tissues.
Cirrhosis is a terminal stage symptom of chronic hepatitis, and highly frequently develops hepatocyte cancer. There is no radical cure except for liver transplantation, and development of a treatment method inducing defibrosis in the stage of hepatic fibrosis before developing cirrhosis is urgently needed.
Patent documents 1, 2 and the like disclose liver fibrosis inhibitors containing a hydroquinone derivative, proanthocyanidin and the like as an active ingredient. These known documents disclose only studies for a suppressive action on liver fibrosis at a cellular level and for an acute cirrhosis model induced by chemical substances such as carbon tetrachloride and the like, and verification using a model showing slow and sustained progression from chronic hepatitis to hepatic fibrosis and cirrhosis, which is caused by hepatitis virus, has not been performed.